Article

Vestibular migraine: clinical aspects and pathophysiology.

Department of Otolaryngology, University of Pittsburgh, Pittsburgh, PA 15213, USA. Electronic address: .
The Lancet Neurology (Impact Factor: 21.82). 07/2013; 12(7):706-15. DOI: 10.1016/S1474-4422(13)70107-8
Source: PubMed

ABSTRACT Vestibular migraine is becoming recognised as a distinct clinical entity that accounts for a high proportion of patients with vestibular symptoms. A temporal overlap between vestibular symptoms, such as vertigo and head-movement intolerance, and migraine symptoms, such as headache, photophobia, and phonophobia, is a requisite diagnostic criterion. Physical examination and laboratory testing are usually normal in vestibular migraine but can be used to rule out other vestibular disorders with overlapping symptoms. The pathophysiology of vestibular migraine is incompletely understood but plausibly could include neuroanatomical pathways to and from central vestibular structures and neurochemical modulation via the locus coeruleus and raphe nuclei. In the absence of controlled trials, treatment options for patients with vestibular migraine largely mirror those for migraine headache.

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    ABSTRACT: Vestibular migraine (VM), a common cause of vestibular symptoms within the general pop-ulation, is a disabling and poorly understood form of dizziness. We sought to examine the underlying pathophysiology of VM with three studies, which involved the central synthesis of canal and otolith cues, and present preliminary results from each of these studies: (1) VM patients appear to have reduced motion perception thresholds when canal and otolith signals are modulated in a co-planar manner during roll tilt; (2) percepts of roll tilt appear to develop more slowly in VM patients than in control groups during a centrifugation par-adigm that presents conflicting, orthogonal canal and otolith cues; and (3) eye movement responses appear to be different in VM patients when studied with a post-rotational tilt paradigm, which also presents a canal–otolith conflict, as the shift of the eye's rotational axis was larger in VM and the relationship between the axis shift and tilt suppression of the vestibulo-ocular reflex differed in VM patients relative to control groups. Based on these preliminary perceptual and eye movement results obtained with three different motion paradigms, we present a hypothesis that the integration of canal and otolith signals by the brain is abnormal in VM and that this abnormality could be cerebellar in origin. We provide potential mechanisms that could underlie these observations, and speculate that one of more of these mechanisms contributes to the vestibular symptoms and motion intolerance that are characteristic of the VM syndrome.
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